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Purpose: This work investigates the hypothesis that genetic background plays a significant role in the signalling mechanisms underlying induction and perpetuation of genomic instability following radiation exposure. Materials and methods:Bone marrow from two strains of mice (CBA and C57), were exposed to a range of X-ray doses (0, 0.01, 0.1, 1 and 3 Gy). Different cellular signalling endpoints: apoptosis, cytokine levels and calcium flux, were evaluated at 2h, 24h and 7d post-irradiation to evaluate immediate and delayed effects.Results: In CBA (radio-sensitive) elevated apoptosis levels were observed at 24h post X-irradiation, transforming growth factor-β (TGF-β) levels were additionally shown to increase with time and dose. C57 showed a higher background level of apoptosis compared to CBA, which was sustained 7 days after radiation exposure. Levels of tumor necrosis factor-α (TNF-α) were also increased at day 7 for higher X-ray doses. TGF-β levels were higher in CBA, whilst C57 exhibited a greater TNF-α response.Calcium flux was induced in reporter cells on exposure to conditioned media from both strains. Conclusions:These results show genetic and dose specific differences in radiation-induced signalling in the initiation and perpetuation of the instability process, which have potential implications on evaluation of non-targeted effects in radiation risk assessment.3

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